CD8 T 细胞耗竭已被确定为三阴性乳腺癌 (TNBC) 免疫抑制和免疫逃逸的重要因素。细胞耗竭导致的功能障碍的特点是效应能力降低和抑制性受体 (IR) 持续表达。导致 CD8 T 细胞耗竭的因素是多方面的，包括外部影响，例如 IR 上调、效应细胞因子减少，以及免疫细胞内部变化，包括转录组改变、表观遗传景观重塑和代谢组变化。 TNBC 肿瘤微环境 (TME) 改变对 Tex 的影响也是一个重要的考虑因素。耗竭型 CD8 T 细胞 (CD8 Tex) 的产生与 TNBC 患者的不良预后和免疫治疗反应率降低呈正相关，这强调了迫切需要开发针对 CD8 T 细胞耗竭机制的新型 TNBC 免疫治疗策略。本综述描绘了 TNBC 中 CD8 T 细胞耗竭发展的动态轨迹，提供了了解其发病机制的最新研究进展的最新信息，并提供了对潜在免疫治疗策略的见解。版权所有 © 2024。由 Elsevier B.V. 出版。

CD8+ T-cell exhaustion has been identified as a significant contributor to immunosuppression and immune escape in triple-negative breast cancer (TNBC). Dysfunction due to cell exhaustion is characterized by reduced effector capacity and sustained expression of inhibitory receptors (IRs). The factors contributing to CD8+ T-cell exhaustion are multifaceted, encompassing external influences such as the upregulation of IRs, reduction of effector cytokines, and internal changes within the immune cell, including transcriptomic alterations, epigenetic landscape remodeling, and metabolomic shifts. The impact of the altered TNBC tumor microenvironment (TME) on Tex is also a critical consideration. The production of exhausted CD8+ T-cells (CD8+ Tex) is positively correlated with poor prognosis and reduced response rates to immunotherapy in TNBC patients, underscoring the urgent need for the development of novel TNBC immunotherapeutic strategies that target the mechanisms of CD8+ T-cell exhaustion. This review delineates the dynamic trajectory of CD8+ T-cell exhaustion development in TNBC, provides an update on the latest research advancements in understanding its pathogenesis, and offers insights into potential immunotherapeutic strategies.Copyright © 2024. Published by Elsevier B.V.